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J Roca

Publications and source records attributed to J Roca.

At least 271 records · Page 15Linked to original sources
PubMed1989

Dissociation of maximal O2 uptake from O2 delivery in canine gastrocnemius in situ.

To test the hypothesis that maximal O2 uptake (VO2max) can be limited by O2 diffusion in the peripheral tissue, we kept O2 delivery [blood flow X arterial O2 content (CaO2)] to maximally contracting muscle equal between 1) low flow-high CaO2 and 2) high flow-low CaO2 conditions. The hypothesis predicts, because of differences in the capillary PO2 profile, that the former condition will result in both a higher VO2max and muscle effluent venous PO2 (PVO2). We studied the relations among VO2max, PVO2, and O2 delivery during maximal isometric contractions in isolated, in situ dog gastrocnemius muscle (n = 6) during these two conditions. O2 delivery was matched by varying arterial O2 partial pressure and adjusting flow to the muscle accordingly. A total of 18 matched O2 delivery pairs were obtained. As planned, O2 delivery was not significantly different between the two treatments. In contrast, VO2max was significantly higher [10.4 +/- 0.5 (SE) ml.100 g-1.min-1; P = 0.01], as was PVO2 (25 +/- 1 Torr; P less than 0.01) in the low flow-high CaO2 treatment compared with the high flow-low CaO2 treatment (9.1 +/- 0.4 ml.100 g-1.min-1 and 20 +/- 1 Torr, respectively). The rate of fatigue was greater in the high flow-low CaO2 condition, as was lactate output from the muscle and muscle lactate concentration. The results of this study show that VO2max is not uniquely dependent on O2 delivery and support the hypothesis that VO2max can be limited by peripheral tissue O2 diffusion.

Acid-Base Equilibrium↗
PubMed1989

Evidence for tissue diffusion limitation of VO2max in normal humans.

We recently found [at approximately 90% maximal O2 consumption (VO2max)] that as inspiratory PO2 (PIO2) was reduced, VO2 and mixed venous PO2 (PVO2) fell together along a straight line through the origin, suggesting tissue diffusion limitation of VO2max. To extend these observations to VO2max and directly examine effluent venous blood from muscle, six normal men cycled at VO2max while breathing air, 15% O2 and 12% O2 in random order on a single day. From femoral venous, mixed venous, and radial arterial samples, we measured PO2, PCO2, pH, and lactate and computed mean muscle capillary PO2 by Bohr integration between arterial (PaO2) and femoral venous PO2 (PfvO2). VO2 and CO2 production (VCO2) were measured by expired gas analysis, VO2max averaged 61.5 +/- 6.2 (air), 48.6 +/- 4.8 (15% O2), and 38.1 +/- 4.1 (12% O2) ml.kg-1.min-1. Corresponding values were 16.8 +/- 5.6, 14.4 +/- 5.0, and 12.0 +/- 5.0 Torr for PfVO2; 23.6 +/- 3.2, 19.1 +/- 4.2, and 16.2 +/- 3.5 Torr for PVO2; and 38.5 +/- 5.4, 30.3 +/- 4.1, and 24.5 +/- 3.6 Torr for muscle capillary PO2 (PmCO2). Each of the PO2 variables was linearly related to VO2max (r = 0.99 each), with an intercept not different from the origin. Similar results were obtained when the subjects were pushed to a work load 30 W higher to ensure that VO2max had been achieved. By extending our prior observations 1) to maximum VO2 and 2) by direct sampling of femoral venous blood, we conclude that tissue diffusion limitation of VO2max may be present in normal humans. In addition, since PVO2, PfVO2, and PmCO2 all linearly relate to VO2max, we suggest that whichever of these is most readily obtained is acceptable for further evaluation of the hypothesis.

Adult↗
PubMed1989

Effects of altitude acclimatization on pulmonary gas exchange during exercise.

Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.

Acclimatization↗
PubMed1989

Pulmonary hemodynamics and gas exchange during exercise in liver cirrhosis.

We have recently shown that ventilation-perfusion (VA/Q) mismatching at rest in cirrhosis is due to an abnormal pulmonary vascular tone. It has been suggested that in patients with cirrhosis, O2 transfer might become diffusion-limited during exercise. This study examined pulmonary hemodynamics and mechanisms modulating gas exchange during exercise (60 to 70% VO2max) in six patients (41 +/- 5 yr, mean +/- SEM) with cirrhosis but with normal lung function tests. At rest, QT was high (8.4 +/- 0.5 L/min), pulmonary vascular resistance (PVR) was low (0.61 +/- 0.17 mm Hg/L/min), and there was mild to moderate VA/Q mismatching (LogSD Q, 0.79 +/- 0.09; normal range, 0.3 to 0.6). However, hyperventilation (PaCO2, 29 +/- 2 mm Hg) and high QT (thus, high PVO2, 41 +/- 2 mm Hg) contributed to the maintenance of PaO2 within normal values (99 +/- 7 mm Hg). Exercise VO2 (1,278 +/- 122 ml/min) was normal relative to work load, but, contrary to that in normal subjects, QT was higher and PVR did not fall. During exercise, PaO2 showed a trend to decrease (to 90 +/- 5 mm Hg) and PaCO2 to rise (to 35 +/- 2 mm Hg), but the differences failed to reach statistical significance (p = 0.07 each). PVO2 fell significantly with exercise (41 +/- 2 to 33 +/- 0.3 mm Hg, p less than 0.05), but neither AaPO2 (15 +/- 7 to 21 +/- 6 mm Hg) nor VA/Q inequality (LogSD Q, 0.82 +/- 0.11) changed. No systemic difference was noticed between predicted and measured PaO2 values, suggesting no O2 diffusion impairment during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Mechanisms of hypoxemia in patients with status asthmaticus requiring mechanical ventilation.

Eight consecutive patients (mean +/- SD age, 43 +/- 11 yr) with acute severe asthma (status asthmaticus) requiring assisted ventilation were studied within the first 24 to 48 h of admission, at maintenance FIO2 and while breathing 100% O2, using the multiple inert gas elimination technique. Ventilation-perfusion (VA/Q) inequality was characterized by a marked bimodal blood flow distribution (perfusion to normal and low VA/Q populations) in all but two patients, with a mean of 27.6 +/- 12.3% of the total perfusion present in the low VA/Q ratio units (between 0.1 and 0.005). As a result, the dispersion of pulmonary blood flow distribution (log SDQ) was severely abnormal (mean, 1.65 +/- 0.28; normal range, 0.3 to 0.6). No patient had a substantial shunt (VA/Q = 0) (mean value, 1.5 +/- 2.3%). The ventilation distribution was never bimodal, but the dispersion of the ventilation distribution (log SDV) was moderately elevated (1.01 +/- 0.24). High VA/Q areas (ventilation to VA/Q units between 10 and 100) were generally absent. While breathing 100% O2, PaO2, PvO2, and PaCO2 significantly rose, as did shunt and blood flow dispersion. Patients with life-threatening acute severe asthma treated by mechanical ventilation show: (1) the most abnormal gas exchange characteristics of the VA/Q spectrum observed to date in human asthma but essentially the same pattern as in patients with less severe disease; (2) a high level of hypoxic pulmonary vascular response; (3) a significant amount of shunt while breathing 100% O2, suggesting the presence of absorption atelectasis or redistribution of blood flow.

Adult↗
PubMed1989

Ventilation-perfusion mismatching in chronic obstructive pulmonary disease during ventilator weaning.

Using the multiple inert gas elimination technique, we studied ventilation-perfusion (VA/Q) relationships in eight patients with chronic obstructive pulmonary disease (COPD) during mechanical ventilation (MV) and again during weaning (spontaneous ventilation [SV] through an endotracheal tube) from MV needed for acute respiratory failure. The patients, seven men and one woman with a mean age of 63 +/- 2.8 (SEM) yr (FEV1 33 +/- 5.2% of predicted), required MV for 9.0 +/- 2.4 days prior to the study. The patients were studied at maintenance FIO2 (0.28 to 0.40) while breathing 100% O2, both during MV and SV. After 30 min of SV, PaCO2 increased from 48.9 +/- 3.4 to 58.3 +/- 3.1 mm Hg (p = 0.003) and pH decreased from 7.42 +/- 0.01 to 7.36 +/- 0.01 (p = 0.001) without significant changes in PaO2. Despite a decrease in tidal volume (VT) from 700.0 +/- 41.1 during MV to 313.0 +/- 39.6 ml during SV (p = 0.001), minute ventilation remained unchanged (from 8.2 +/- 0.7 during MV to 7.4 +/- 0.6 L/min during SV). Furthermore, cardiac output (QT), oxygen delivery (QO2), and mixed venous PO2 (PVO2) significantly rose during SV when compared with the MV (QT: from 4.7 +/- 0.4 to 6.7 +/- 0.7 L/min, p = 0.011; QO2: from 857.3 +/- 113.0 to 1078.5 +/- 158.9 ml/min, p = 0.0074; PVO2: from 36.7 +/- 1.1 to 42.3 +/- 2.2 mm Hg, p = 0.041). Overall VA/Q inequality worsened as blood flow was redistributed to low VA/Q areas (from 9.4 +/- 4.4 to 19.6 +/- 5.3% of QT, p = 0.05). The dispersion of the ventilation distribution (log SDV) significantly worsened during SV (from 1.0 +/- 0.08 during MV to 1.2 +/- 0.08 during SV, p = 0.044). No changes were observed in either series dead space or ventilation of high VA/Q ratio units.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Lung function in allogeneic bone marrow transplantation recipients.

In order to investigate the incidence of pulmonary function complications following bone marrow transplantation (BMT), 17 patients with leukaemia and 8 with aplastic anaemia were sequentially assessed over a one year period. Before BMT, all the patients were free of respiratory symptoms and had both normal chest X-ray and routine lung function tests. However, 5 patients disclosed airway hyperreactivity. Aplastic anaemia patients had significantly lower haemoglobin-adjusted diffusing capacity for carbon monoxide (DLCO) than those with leukaemia, a finding significantly related to the lower haemoglobin values shown in the former individuals. Following BMT there were transient mild to moderate reductions in DLCO and static lung volumes; moreover, patients with leukaemia had lower DLCO than those with aplastic anaemia. Fourteen of the 25 patients had ventilatory defects, including 10 individuals with bronchial hyperresponsiveness. Post-BMT lung function changes were transiently accompanied by mild to moderate symptoms of respiratory disease in most of the patients.

Adult↗
PubMed1989

Direct repair of spondylolysis.

Fifteen patients with spondylolysis have received compression screw and bone graft treatment for repair of this defect. In all but one case, solid fusion of the pars defect was achieved within six months after surgery. After one year, 13 of the 15 patients were able to participate fully in sports activities.

Adolescent↗
PubMed1989

[Pericardiocentesis: usefulness in the routine determination of intrapericardial pressure].

The usefulness of routine intrapericardial pressure determination and hemodynamic monitoring during therapeutic (n = 22) or diagnostic (n = 2) pericardiocentesis was analyzed. Hemodynamic data confirmed the presence of cardiac tamponade in all cases, including the 2 patients without clinical suspicion. Prior to fluid evacuation, abnormally elevated levels of intrapericardial (13 +/- 5 mmHg), right atrial (14 +/- 4 mmHg) and pulmonary capillary (16 +/- 3 mmHg) pressures were observed. A significant correlation was found between intrapericardial and right atrial pressures (r = 0.97, p less than 0.05) and also between intrapericardial and pulmonary capillary pressures (r = 0.69, p less than 0.05). The basal cardiac output was low (3 +/- 1 l/min) and increased after the pericardiocentesis in all but one patient. According to the results of pericardiocentesis, patients were classified into three groups. Group I: intrapericardial and right atrial pressures decreased to normal levels. The increment of cardiac output was high (72%) and the procedure was considered successful. Group II: right atrial and intrapericardial pressures remained elevated (7.7 +/- 4 and 7 +/- 2 mmHg, respectively) and the cardiac output increment was less marked (52%), thus indicating incomplete drainage. Group III: intrapericardial pressure decreased to normal levels but right atrial pressure remained elevated. All these patients were found to have associated cardiac disease, most frequently constriction. We conclude that routine determination of intrapericardial pressure: 1) reveals the presence of tamponade in cases without clinical suspicion; 2) indicates the efficacy of drainage; and 3) together with right atrial pressure recording, provides early diagnosis of associated cardiac disease, especially effusive-constrictive pericarditis.

Adult↗
PubMed1988

Limitation of maximal O2 uptake and performance by acute hypoxia in dog muscle in situ.

The factors that determine maximal O2 uptake (VO2max) and muscle performance during severe, acute hypoxemia were studied in isolated, in situ dog gastrocnemius muscle. Our hypothesis that VO2max is limited by O2 diffusion in muscle predicts that decreases in VO2max, caused by hypoxemia, will be accompanied by proportional decreases in muscle effluent venous PO2 (PvO2). By altering the fraction of inspired O2, four levels of arterial PO2 (PaO2) [21 +/- 2, 28 +/- 1, 44 +/- 1, and 80 +/- 2 (SE) Torr] were induced in each of eight dogs. Muscle arterial and venous circulation was isolated and arterial pressure held constant by pump perfusion. Each muscle worked maximally (3 min at 5-6 Hz, isometric twitches) at each PaO2. Arterial and venous samples were taken to measure lactate, [H+], PO2, PCO2, and muscle VO2. Muscle biopsies were taken to measure [H+] (homogenate method) and lactate. VO2max decreased with PaO2 and was linearly (R = 0.99) related to both PVO2 and O2 delivery. As PaO2 fell, fatigue increased while muscle lactate and [H+] increased. Lactate release from the muscle did not change with PaO2. This suggests a barrier to lactate efflux from muscle and a possible cause of the greater fatigue seen in hypoxemia. The gas exchange data are consistent with the hypothesis that VO2max is limited by peripheral tissue diffusion of O2.

Acid-Base Equilibrium↗
PubMed1988

Serial relationships between ventilation-perfusion inequality and spirometry in acute severe asthma requiring hospitalization.

Patterns of VA/Q distribution and their relationship to spirometric indices were studied in 10 patients with acute severe asthma requiring hospitalization (7 women and 3 men 41.0 +/- 5.6 yr of age, mean +/- SEM) on admission and during subsequent recovery. On admission, all patients received the standard therapeutic regimen for our hospital. Spirometry and essentially noninvasive multiple inert gas elimination measurements were obtained serially, approximately once every day, whereas conventional arterial blood gases were determined every 3 days. On admission, all patients showed severe air-flow obstruction (FEV1/FVC% = 34.1 +/- 4.3%) and moderate to severe hypoxemia without CO2 retention (PaO2 = 50.5 +/- 2.6 mm Hg; PaCO2 = 37.1 +/- 2.4 mm Hg; AaPO2 = 53.7 +/- 3.0 mm Hg). Nine of the 10 patients showed bimodal blood flow distributions (dispersion of blood flow distribution, log SD Q = 1.34 +/- 0.11; normal range, 0.3 to 0.6) with only small amounts of shunt (1.09 +/- 0.8%). However, no significant interindividual correlations were observed between maximal expiratory flow rates (FEV1 and FEF25(-75) and log SD Q (r2 = 0.14 and 0.006, respectively). This lack of correlation persisted throughout hospitalization. Despite both clinical and spirometric improvement in all patients, there was simultaneous improvement in VA/Q matching in only one patient. Statistically significant negative correlations between maximal expiratory flow rates and gas exchange did develop toward the end of the study (Weeks 3 and 4 after discharge) when maximal recovery of physiologic changes associated with the acute asthma attack was achieved.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1988

Effect of almitrine on ventilation-perfusion distribution in adult respiratory distress syndrome.

Almitrine improves ventilation/perfusion relationships (VA/Q) in COPD, but its effects in ARDS, in which VA/Q mismatching is the cause of severe hypoxemia, are not known. The effects of almitrine on pulmonary gas exchange and circulation were assessed in 9 patients with ARDS who were sedated, paralyzed, and mechanically ventilated at constant FlO2 (range, 0.48 to 0.74). Systemic and pulmonary hemodynamics, conventional gas exchange, and the VA/Q distribution by the multiple inert gas elimination technique (MIGT) were measured before (baseline), during (ALM 15), at the end of (ALM 30), and at 30-min intervals after (POSTALM 30, 60, and 90) the intravenous infusion of 0.5 mg/kg body weight of almitrine over 30 min. Almitrine significantly increased PaO2 from 78 +/- 15 mm Hg to 140 +/- 49 at ALM 15 and 138 +/- 52 at ALM 30. AaPO2 and QS/QT decreased during the administration of the drug. The MIGT showed that almitrine redistributed pulmonary blood flow from shunt areas (reduction from 29 +/- 11 to 17 +/- 11% of QT) to lung units with normal VA/Q ratios (increase from 63 +/- 9 to 73 +/- 6% of QT). The Ppa increased from 26 +/- 5 to 30 +/- 5 mm Hg without changes in QT. Changes were transient, returning toward baseline 30 min after stopping the infusion of the drug. Almitrine significantly reduced the VA/Q inequalities present in ARDS and may be useful in the management of those patients.

Adult↗
PubMed1988

Different patterns of gas exchange response to exercise in asbestosis and idiopathic pulmonary fibrosis.

To analyse the pattern of pulmonary gas exchange during maximal exercise (Emax) in asbestosis, we compared nine subjects with this disease (1 female/8 male), aged 54 +/- 11 yrs (mean +/- SD), to nine patients (1 female/8 male) with idiopathic pulmonary fibrosis (IPF) of a similar age, height, weight and smoking history, both at rest and during Emax. No differences were observed in dynamic and static lung volumes between the groups. However, patients with IPF had a lower DLCOsb and KCO (p less than 0.005 and 0.05, respectively). At rest, both groups showed mild arterial hypoxaemia (76 +/- 11, asbestosis, vs 77 +/- 11 mmHg, IPF), widened AaPO2 (32 +/- 14 vs 31 +/- 13 mmHg) and slight increases in VD/VT (47 +/- 12 vs 46 +/- 11%), respectively. During Emax, PaO2 fell to 51 +/- 7 mmHg in patients with IPF whereas those with asbestosis had PaO2 of 73 +/- 21 mmHg (p less than 0.05). Conversely, those with asbestosis were able to reduce VD/VT (from 47 +/- 12 to 39 +/- 10%, p = 0.01) as opposed to those with IPF (from 46 +/- 11 to 47 +/- 13%). Furthermore, DLCOsb and AaPO2 during Emax were highly correlated only in IPF (r: -0.84, p less than 0.01). Despite the finding that both diseases represent a diffuse pulmonary fibrosis with a similar degree of resting ventilatory impairment, the pattern of gas exchange during exercise is different in each. These differences may be related to the underlying morphology of each process, which probably includes more airway disease and less pulmonary vascular involvement and/or a different degree of interstitial fibrotic change in asbestosis.

Asbestosis↗
PubMed1988

Lung function changes following Legionnaires' disease.

Eleven out of thirteen patients hospitalized because of severe pneumonia caused by Legionella Pneumophila were evaluated over a period of 53 months. During the acute phase, all but one patient manifested severe hypoxaemia, needing either supplementary oxygen or, in the case of three, mechanical ventilation and one died. Following recovery, two patients complained of mild shortness of breath alone. However, most of the individuals showed subclinical mild to moderate ventilatory and/or gas exchange abnormalities a few months after discharge (less than 6 months). Despite the fact that some of these functional findings in part persisted at long-term (6-33 months), a significant overall improvement in lung function was noticed. The main pulmonary functional sequelae following Legionnaires' Disease might include a restrictive ventilatory defect, a low transfer factor and hypoxaemia.

Acute Disease↗
PubMed1987

Rifampin for eradicating carriage of multiply resistant Haemophilus influenzae b.

We studied the efficacy of rifampin prophylaxis in reducing the prevalence of ampicillin- and chloramphenicol-resistant Haemophilus influenzae type b in four day care facilities after each center had individual cases of invasive infections (two meningitis, one pneumonia and one cellulitis) caused by multiply resistant organisms. Rifampin was given in a single daily dose of 20 mg/kg for 4 days. Cultures were taken pretreatment and 10 days after the last dose of rifampin. Included in the study were 174 children and 27 adults. We identified a total of 55 nasopharyngeal carriers; 45 received rifampin and 10 refused treatment. On the 10-day follow-up culture in the second sample, 95.5 and 20%, respectively, of treated and untreated children were no longer colonized with H. influenzae (P less than 0.001, Fisher's exact test). We conclude that rifampin can successfully reduce the prevalence of multiply resistant H. influenzae type b carriers attending day care centers.

Adult↗
PubMed1987

Bronchoalveolar lavage cellular analysis and gallium lung scan in the assessment of patients with amiodarone-induced pneumonitis.

Seven patients suffering from amiodarone-induced pneumonitis were followed after diagnosis over a period of 16 +/- 6 months. All of them showed clinical, radiographic and functional manifestations of interstitial lung disease. Bronchoalveolar lavage was performed on 6 of them and disclosed lymphocytosis in 2 cases (associated to eosinophilia in 1 of them), neutrophilia in 1 and normal differential count in 2. In 1 case there were abundant hemosiderin-laden macrophages. In addition, all patients evidenced an increased 67Ga lung scan uptake. After discontinuation of amiodarone therapy (with or without corticosteroid therapy), 67Ga lung uptake normalized in 3 cases, but remained increased in 3. Bronchoalveolar lavage was repeated only in 2 cases, showing disappearance of lymphocytosis in one and abundant hemosiderin-laden macrophages in the other. Our results suggest that (1) hemosiderin-laden macrophages can be found in bronchoalveolar lavage in patients with amiodarone-induced pneumonitis, probably related to subclinical chronic left-sided heart failure; (2) 67Ga lung scan appears to be a sensitive marker of amiodarone pneumonitis, although it can remain abnormal after pulmonary clinical, radiographic and functional normalization.

Adult↗